Journal
CELL REPORTS
Volume 24, Issue 10, Pages 2561-+Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2018.08.004
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Funding
- Alberta Innovates Health Solutions (AIHS) grant [201200859]
- CIHR New Investigator Award
- Alberta Children's Health Research Institute Fellowship
- Alberta Innovates Health Solutions Scholarship
- BSc Neuroscience Undergraduate Research Scholarship
- CIHR grant
- AIHS
- CIHR
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Pro-regenerative macrophages are well known for their role in promoting tissue repair; however, their specific roles in promoting regeneration of the injured nerve are not well defined. Specifically, how macrophages interact with Schwann cells following injury during remyelination has been largely unexplored. We demonstrate that after injury, including in humans, macrophages function to clear debris and persist within the nerve microenvironment. Macrophage ablation immediately preceding remyelination results in an increase in immature Schwann cell density, a reduction in remyelination, and long-term deficits in conduction velocity. Targeted RNA-seq of macrophages from injured nerve identified Gas6 as one of several candidate factors involved in regulating Schwann cell dynamics. Functional studies show that the absence of Gas6 within monocyte lineage cells impairs Schwann cell remyelination within the injured nerve. These results demonstrate a role for macrophages in regulating Schwann cell function during nerve regeneration and highlight a molecular mechanism by which this occurs.
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